Xeroderma Pigmentosum Group A Protein

"Xeroderma Pigmentosum Group A Protein" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings). Descriptors are arranged in a hierarchical structure, which enables searching at various levels of specificity.

MeSH information

Definition | Details | More General Concepts | Related Concepts | More Specific Concepts

A ZINC FINGER MOTIF protein that recognizes and interacts with damaged DNA. It is a DNA-binding protein that plays an essential role in NUCLEOTIDE EXCISION REPAIR. Mutations in this protein are associated with the most severe form of XERODERMA PIGMENTOSUM.

Descriptor ID

D051760

MeSH Number(s)

D12.776.260.975

Concept/Terms

Xeroderma Pigmentosum Group A Protein

Below are MeSH descriptors whose meaning is more general than "Xeroderma Pigmentosum Group A Protein".

Chemicals and Drugs [D]
Amino Acids, Peptides, and Proteins [D12]
Proteins [D12.776]
DNA-Binding Proteins [D12.776.260]
Xeroderma Pigmentosum Group A Protein [D12.776.260.975]

Below are MeSH descriptors whose meaning is related to "Xeroderma Pigmentosum Group A Protein".

Below are MeSH descriptors whose meaning is more specific than "Xeroderma Pigmentosum Group A Protein".

publications

Timeline | Most Recent

This graph shows the total number of publications written about "Xeroderma Pigmentosum Group A Protein" by people in Harvard Catalyst Profiles by year, and whether "Xeroderma Pigmentosum Group A Protein" was a major or minor topic of these publication.

Bar chart showing 10 publications over 8 distinct years, with a maximum of 2 publications in 2006 and 2007

To see the data from this visualization as text, click here.

Year	Major Topic	Minor Topic	Total
1994	0	1	1
2002	0	1	1
2006	1	1	2
2007	2	0	2
2009	0	1	1
2011	0	1	1
2015	0	1	1
2021	1	0	1

Below are the most recent publications written about "Xeroderma Pigmentosum Group A Protein" by people in Profiles.

Neurovascular dysfunction and neuroinflammation in a Cockayne syndrome mouse model. Aging (Albany NY). 2021 10 10; 13(19):22710-22731.

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Defining the Contribution of MC1R Physiological Ligands to ATR Phosphorylation at Ser435, a Predictor of DNA Repair in Melanocytes. J Invest Dermatol. 2015 Dec; 135(12):3086-3095.

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Up-regulation of nucleotide excision repair in mouse lung and liver following chronic exposure to aflatoxin B1 and its dependence on p53 genotype. Toxicol Appl Pharmacol. 2014 Mar 01; 275(2):96-103.

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The molecular basis of CRL4DDB2/CSA ubiquitin ligase architecture, targeting, and activation. Cell. 2011 Nov 23; 147(5):1024-39.

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Recruitment of fanconi anemia and breast cancer proteins to DNA damage sites is differentially governed by replication. Mol Cell. 2009 Sep 11; 35(5):716-23.

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Nucleotide excision repair driven by the dissociation of CAK from TFIIH. Mol Cell. 2008 Jul 11; 31(1):9-20.

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Structural basis for the recruitment of ERCC1-XPF to nucleotide excision repair complexes by XPA. EMBO J. 2007 Nov 14; 26(22):4768-76.

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Polymorphisms in nucleotide excision repair genes, polycyclic aromatic hydrocarbon-DNA adducts, and breast cancer risk. Cancer Epidemiol Biomarkers Prev. 2007 Oct; 16(10):2033-41.

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Polymorphisms in nucleotide excision repair genes, arsenic exposure, and non-melanoma skin cancer in New Hampshire. Environ Health Perspect. 2007 Aug; 115(8):1231-6.

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Increased expression of p53 enhances transcription-coupled repair and global genomic repair of a UVC-damaged reporter gene in human cells. DNA Repair (Amst). 2007 May 01; 6(5):588-601.

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Environ Health Perspect
EMBO J
Carcinogenesis
Aging (Albany NY)
Mol Cell
FASEB J
Eur J Biochem
DNA Repair (Amst)
Cell
Cancer Epidemiol Biomarkers Prev